TY  - JOUR
AU  - Wang, Xiaoliang
AU  - Dai, James Y
AU  - Albanes, Demetrius
AU  - Arndt, Volker
AU  - Berndt, Sonja I
AU  - Bézieau, Stéphane
AU  - Brenner, Hermann
AU  - Buchanan, Daniel D
AU  - Butterbach, Katja
AU  - Caan, Bette
AU  - Casey, Graham
AU  - Campbell, Peter T
AU  - Chan, Andrew T
AU  - Chen, Zhengyi
AU  - Chang-Claude, Jenny
AU  - Cotterchio, Michelle
AU  - Easton, Douglas F
AU  - Giles, Graham G
AU  - Giovannucci, Edward
AU  - Grady, William M
AU  - Hoffmeister, Michael
AU  - Hopper, John L
AU  - Hsu, Li
AU  - Jenkins, Mark A
AU  - Joshi, Amit D
AU  - Lampe, Johanna W
AU  - Larsson, Susanna C
AU  - Lejbkowicz, Flavio
AU  - Li, Li
AU  - Lindblom, Annika
AU  - Le Marchand, Loic
AU  - Martin, Vicente
AU  - Milne, Roger L
AU  - Moreno, Victor
AU  - Newcomb, Polly A
AU  - Offitt, Kenneth
AU  - Ogino, Shuji
AU  - Pharoah, Paul D P
AU  - Pinchev, Mila
AU  - Potter, John D
AU  - Rennert, Hedy S
AU  - Rennert, Gad
AU  - Saliba, Walid
AU  - Schafmayer, Clemens
AU  - Schoen, Robert E
AU  - Schrotz-King, Petra
AU  - Slattery, Martha L
AU  - Song, Mingyang
AU  - Stegmaier, Christa
AU  - Weinstein, Stephanie J
AU  - Wolk, Alicja
AU  - Woods, Michael O
AU  - Wu, Anna H
AU  - Gruber, Stephen B
AU  - Peters, Ulrike
AU  - White, Emily
TI  - Mendelian randomization analysis of C-reactive protein on colorectal cancer risk.
JO  - International journal of epidemiology
VL  - 48
IS  - 3
SN  - 1464-3685
CY  - Oxford
PB  - Oxford Univ. Press
M1  - DKFZ-2019-00773
SP  - 767-780
PY  - 2019
AB  - Chronic inflammation is a risk factor for colorectal cancer (CRC). Circulating C-reactive protein (CRP) is also moderately associated with CRC risk. However, observational studies are susceptible to unmeasured confounding or reverse causality. Using genetic risk variants as instrumental variables, we investigated the causal relationship between genetically elevated CRP concentration and CRC risk, using a Mendelian randomization approach.Individual-level data from 30 480 CRC cases and 22 844 controls from 33 participating studies in three international consortia were used: the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), the Colorectal Transdisciplinary Study (CORECT) and the Colon Cancer Family Registry (CCFR). As instrumental variables, we included 19 single nucleotide polymorphisms (SNPs) previously associated with CRP concentration. The SNP-CRC associations were estimated using a logistic regression model adjusted for age, sex, principal components and genotyping phases. An inverse-variance weighted method was applied to estimate the causal effect of CRP on CRC risk.Among the 19 CRP-associated SNPs, rs1260326 and rs6734238 were significantly associated with CRC risk (P = 7.5 × 10-4, and P = 0.003, respectively). A genetically predicted one-unit increase in the log-transformed CRP concentrations (mg/l) was not associated with increased risk of CRC [odds ratio (OR) = 1.04; 95
LB  - PUB:(DE-HGF)16
C6  - pmid:30476131
DO  - DOI:10.1093/ije/dyy244
UR  - https://inrepo02.dkfz.de/record/143174
ER  -